JCI early table of contents for May 15, 2013

For patients with leukemia and other hematological malignancies, transplantation of hematopoietic stem cells (HSCT) can be a powerfully effective therapy. In addition to the desirable anti-tumor effect, transplanted cells can also attack the host tissue, resulting in graft-versus-host disease (GVHD). In this issue of the Journal of Clinical Investigation, Arnab Ghosh and colleagues at Memorial Sloan-Kettering Cancer Center found that expression of a protein that causes cell death, TRAIL, in transplanted cells was critical for an effective anti-tumor response. Immune cells engineered to express higher levels of TRAIL killed the cells that cause GVHD and increased anti-tumor activity. In an accompanying commentary, Nelson Chao suggests that new therapeutics may take advantage of TRAIL-expressing cells to promote an anti-tumor response without putting patients at risk for GVHD.

Researchers identify signals that direct the immune system to reject a transplanted organ

Organ transplant rejection occurs when the transplant recipient's immune system identifies the transplanted organ as foreign tissue and attacks it. It was previously thought that T cells, the immune cells that mediate rejection, must first be activated by molecules known as chemokines in order to migrate to the transplanted organ. In this issue of the Journal of Clinical Investigation, Fadi Lakkis and colleagues at the University of Pittsburgh used mice to demonstrate that chemokine stimulation of T cells is not required for migration. Instead, these cells must come into contact with immune-stimulating proteins (antigens) that are specifically expressed by the transplanted organ. In an accompanying commentary, Terry Strom discusses how these findings could have important implications for the design of novel anti-rejection therapeutics.

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